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Frequency Foundation

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Alzheimers – Replacing the Missing Gamma Frequency

Unique visual stimulation may be new treatment for Alzheimer’s

Noninvasive technique reduces beta amyloid plaques in mouse models of Alzheimer’s disease.Watch Video

Anne Trafton | MIT News Office
December 7, 2016

In a study of mice that were genetically programmed to develop Alzheimer’s but did not yet show any plaque accumulation or behavioral symptoms, Tsai and her colleagues found impaired gamma oscillations during patterns of activity that are essential for learning and memory while running a maze.

Next, the researchers stimulated gamma oscillations at 40 hertz in a brain region called the hippocampus, which is critical in memory formation and retrieval. These initial studies relied on a technique known as optogenetics, co-pioneered by Boyden, which allows scientists to control the activity of genetically modified neurons by shining light on them. Using this approach, the researchers stimulated certain brain cells known as interneurons, which then synchronize the gamma activity of excitatory neurons.

After an hour of stimulation at 40 hertz, the researchers found a 40 to 50 percent reduction in the levels of beta amyloid proteins in the hippocampus. Stimulation at other frequencies, ranging from 20 to 80 hertz, did not produce this decline.

Gamma frequency entrainment attenuates amyloid load and modifies microglia

Nature 540, 230–235 (08 December 2016) doi:10.1038/nature20587

Changes in gamma oscillations (20–50 Hz) have been observed in several neurological disorders. However, the relationship between gamma oscillations and cellular pathologies is unclear. Here we show reduced, behaviourally driven gamma oscillations before the onset of plaque formation or cognitive decline in a mouse model of Alzheimer’s disease. Optogenetically driving fast-spiking parvalbumin-positive (FS-PV)-interneurons at gamma (40 Hz), but not other frequencies, reduces levels of amyloid-β (Aβ)1–40 and Aβ 1–42 isoforms. Gene expression profiling revealed induction of genes associated with morphological transformation of microglia, and histological analysis confirmed increased microglia co-localization with Aβ. Subsequently, we designed a non-invasive 40 Hz light-flickering regime that reduced Aβ1–40 and Aβ1–42 levels in the visual cortex of pre-depositing mice and mitigated plaque load in aged, depositing mice. Our findings uncover a previously unappreciated function of gamma rhythms in recruiting both neuronal and glial responses to attenuate Alzheimer’s-disease-associated pathology.

Biofilms Version 7.0

 Biofilms – Version 7.0 is the 1917 release of hundreds of biofilm programs. Thousands of updates and many more bacterial strains have been added.  Use of the new Hunter 4025 scanning technology has allowed more precise identification of specific pathogens in some cases.
Most of the 600 strains of periodontal biofilms DNA sequenced by the National Institutes of Health are now  in this series of programs. Most strains of lyme disease borrelia are included. Nanobacteria and other biofilms associated with Altzheimers can be found here. Biofilms are associated with all major disease categories. There is even a new program targets abdominal fat.
Recent research has focused on biofilm involvement in tumors. All tumors (benign and malignant) are infected with biofilms. The relationship of causation of tumors by biofilms is still being researched. It appears that many so-called Rife frequencies are really components of biofilms.
There is extensive academic research on biofilms. See Montana State University Center for Biofilm Engineering for the basics, as well as access to papers from dozens of conferences. For example, most people have biofilms forming calcification in their joints and articles. Here is a photo of such a biofilm on a grain of sand:
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These biofioms are not doing your heart any good.
Most bacteria infections today are antibiotic resistant biofilms. While over 600 species of these biofilms have been DNA sequenced for periodontal disease, these gum infections are the tip of the iceberg. A huge amount of illness from joint problems to wound infections to heart disease are caused by biofilms.
During the past two years, intensive research at the Frequency Research Foundation has developed frequency sequences for about 400 biofilms. A notable finding is that radical reduction in blood pressure can be achieved by running the appropriate borrelia biofilm programs for infected individuals. All people exposed to lyme disease will need them.
January 2005, National Institute of Dental and Craniofacial Research
It has long been assumed that all chronic periodontitis is the same no matter where one lives in the world.  But some scientists have wondered whether the bacterial composition of the oral biofilm – the sticky, mat-like microbial communities that form on our teeth and cause chronic periodontitis – might vary geographically.  In the November issue of the Journal of Clinical Periodontology, NIDCR grantees and their colleagues report for the first time that this is indeed the case.  In a study of more than 300 patients with chronic periodontitis from Sweden, the United States, Brazil, and Chile, they found clear geographical differences in the bacterial content of dental plaque obtained from the periodontal lesions.  To hear more about this important paper, the Inside Scoop recently talked with lead author Anne Haffajee, B.D.S., and Sigmund Socransky, D.D.S., the senior author. Both are scientists at The Forsyth Institute in Boston.

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Work on biofilms is becoming as extensive as previous work on lyme disease frequencies. Daily updates indicate that they are at the root of much of heart disease, respiratory problems, joint issues, prostate problems, and tumors of all types. Recent releases added many biofilms seen with abnormal cells in cancer patients, raising the question as to whether they are involved in carcinogenesis.

There are over 600 species of periodontal biofilms that have been DNA sequenced. During the past two years, the Frequency Research Foundation has expanded detailed analysis of  frequencies for many more biofilm infections. This is the most extensive research effort since development of the lyme disease frequency sets and has involved daily analysis and update of biofilm frequencies from September 2011 until July 2013. As a result these data are the most comprehensive biofilm frequency sets available.

Some are based on the lyme borellia spirochete and cause elevated blood pressure. Others are directly related to mortality from heart disease.

See:

Persistent Chlamydia pneumoniae infection of cardiomyocytes is correlated with fatal myocardial infarction.
Spagnoli LG, Pucci S, Bonanno E, Cassone A, Sesti F, Ciervo A, Mauriello A.

All biofilms can go systemic in the body and cause a wide variety of symptoms and disease outcomes. For the first time it is possible to work on getting rid of the root cause of gum disease and other persistent infections.

Frequencies are published as a set of over a dozen F165 program files. It is best to work on one biofilm frequency set at a time as one clinician has noted that use of these frequencies is analogous to tearing up the floorboards in your house. You never know what you are going to find underneath.

Biofilm frequencies are available to subscribers.

Alzheimer’s and Herpes simplex virus

Herpes simplex virus type 1 DNA is located within Alzheimer’s disease amyloid plaques.

Faculty of Life Sciences, University of Manchester, UK.

Abstract

The brains of Alzheimer’s disease sufferers are characterized by amyloid plaques and neurofibrillary tangles. However, the cause(s) of these features and those of the disease are unknown, in sporadic cases. We previously showed that herpes simplex virus type 1 is a strong risk factor for Alzheimer’s disease when in the brains of possessors of the type 4 allele of the apolipoprotein E gene (APOE-epsilon4), and that beta-amyloid, the main component of plaques, accumulates in herpes simplex virus type 1-infected cell cultures and mouse brain. The present study aimed to elucidate the relationship of the virus to plaques by determining their proximity in human brain sections. We used in situ polymerase chain reaction to detect herpes simplex virus type 1 DNA, and immunohistochemistry or thioflavin S staining to detect amyloid plaques. We discovered a striking localization of herpes simplex virus type 1 DNA within plaques: in Alzheimer’s disease brains, 90% of the plaques contained the viral DNA and 72% of the DNA was associated with plaques; in aged normal brains, which contain amyloid plaques at a lower frequency, 80% of plaques contained herpes simplex virus type 1 DNA but only 24% of the viral DNA was plaque-associated (p < 0.001). We suggest that this is because in aged normal individuals, there is a lesser production and/or greater removal of beta-amyloid (Abeta), so that less of the viral DNA is seen to be associated with Abeta in the brain. Our present data, together with our finding of Abeta accumulation in herpes simplex virus type 1-infected cells and mouse brain, suggest that this virus is a major cause of amyloid plaques and hence probably a significant aetiological factor in Alzheimer’s disease. They point to the usage of antiviral agents to treat the disease and possibly of vaccination to prevent it.
Frequencies are available on subscriber’s blog.